At the molecular level, m6A modification mediated by METTL3 promoted the translation of different oncogenic targets including PTEN, c-MYC and BCL2 in the human AML MOLM-13 cell line, whereas METTL3 loss led to an increase in AKT phosphorylation, contributing to the differentiation phenotype (Fig. 3a) [166]. Here, METTL3 is linked to acute myeloid leukemia.